Lopes Thiago R, Sabino-Carvalho Jeann L, Ferreira Thiago H N, Succi José E, Silva Antônio C, Silva Bruno M
Department of Physiology, Federal University of São Paulo, São Paulo, Brazil.
Laboratory of Exercise Physiology, Olympic Center of Training and Research, São Paulo, Brazil.
Front Physiol. 2018 Oct 26;9:1465. doi: 10.3389/fphys.2018.01465. eCollection 2018.
Repeated sprint exercise (RSE) acutely impairs post-exercise heart rate (HR) recovery (HRR) and time-domain heart rate variability (i. e., RMSSD), likely in part, due to lactic acidosis-induced reduction of cardiac vagal reactivation. In contrast, ischemic preconditioning (IPC) mediates cardiac vagal activation and augments energy metabolism efficiency during prolonged ischemia followed by reperfusion. Therefore, we investigated whether IPC could improve recovery of cardiac autonomic control from RSE partially via improved energy metabolism responses to RSE. Fifteen men team-sport practitioners (mean ± SD: 25 ± 5 years) were randomly exposed to IPC in the legs (3 × 5 min at 220 mmHg) or control (CT; 3 × 5 min at 20 mmHg) 48 h, 24 h, and 35 min before performing 3 sets of 6 shuttle running sprints (15 + 15 m with 180° change of direction and 20 s of active recovery). Sets 1 and 2 were followed by 180 s and set 3 by 360 s of inactive recovery. Short-term HRR was analyzed after all sets via linear regression of HR decay within the first 30 s of recovery (T30) and delta from peak HR to 60 s of recovery (HRR60s). Long-term HRR was analyzed throughout recovery from set 3 via first-order exponential regression of HR decay. Moreover, RMSSD was calculated using 30-s data segments throughout recovery from set 3. Energy metabolism responses were inferred via peak pulmonary oxygen uptake ( peak), peak carbon dioxide output ( peak), peak respiratory exchange ratio (RERpeak), first-order exponential regression of decay within 360 s of recovery and blood lactate concentration ([Lac-]). IPC did not change T30, but increased HRR60s after all sets (condition main effect: = 0.03; partial eta square (η ) = 0.27, i.e., large effect size). IPC did not change long-term HRR and RMSSD throughout recovery, nor did IPC change any energy metabolism parameter. In conclusion, IPC accelerated to some extent the short-term recovery, but did not change the long-term recovery of cardiac autonomic control from RSE, and such accelerator effect was not accompanied by any IPC effect on surrogates of energy metabolism responses to RSE.
重复冲刺运动（RSE）会急性损害运动后心率（HR）恢复（HRR）以及时域心率变异性（即，RMSSD），这可能部分是由于乳酸酸中毒导致心脏迷走神经再激活减少。相比之下，缺血预处理（IPC）可介导心脏迷走神经激活，并在长时间缺血后再灌注期间提高能量代谢效率。因此，我们研究了IPC是否可以部分通过改善对RSE的能量代谢反应来促进RSE后心脏自主控制的恢复。15名男子团队运动从业者（平均±标准差：25±5岁）在进行3组每组6次往返跑冲刺（15 + 15米，方向改变180°，主动恢复20秒）前48小时、24小时和35分钟，随机接受腿部IPC（220 mmHg下3×5分钟）或对照（CT；20 mmHg下3×5分钟）。第1组和第2组后进行180秒不活动恢复，第3组后进行360秒不活动恢复。所有组完成后，通过恢复前30秒内HR衰减的线性回归（T30）以及从峰值HR到恢复60秒的变化量（HRR60s）分析短期HRR。通过第3组整个恢复过程中HR衰减的一阶指数回归分析长期HRR。此外，在第3组整个恢复过程中使用30秒数据段计算RMSSD。通过峰值肺摄氧量（ peak）、峰值二氧化碳排出量（ peak）、峰值呼吸交换率（RERpeak）、恢复360秒内 衰减的一阶指数回归以及血乳酸浓度（[Lac-]）推断能量代谢反应。IPC未改变T30，但所有组后HRR60s增加（条件主效应： = 0.03；偏 eta 平方（η ） = 0.27，即大效应量）。IPC在整个恢复过程中未改变长期HRR和RMSSD，也未改变任何能量代谢参数。总之，IPC在一定程度上加速了短期恢复，但未改变RSE后心脏自主控制的长期恢复，且这种加速效应并未伴随着IPC对RSE能量代谢反应替代指标的任何影响。
